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Fuller Albright and our current understanding of calcium and phosphorus regulation and primary hyperparathyroidism.

Abstract
The major contributions of Fuller Albright to our understanding of calcium and phosphorus regulation and primary hyperparathyroidism are highlighted. Albright was the first investigator to initiate a systematic study of mineral metabolism. With resources limited to the measurement of serum calcium and phosphorus and the infusion of parathyroid extract, Albright used balance studies to establish a framework for our understanding of calcium and phosphorus regulation and primary hyperparathyroidism. Albright was the first to show that the etiology of primary hyperparathyroidism could be from either an adenoma or hyperplasia of the parathyroid glands and stone disease was a separate manifestation of primary hyperparathyroidism. Albright also showed that: 1) a renal threshold for calcium excretion was present in hypoparathyroid patients; 2) correction of hypocalcemia in hypoparathyroid patients with vitamin D had a phosphaturic action; 3) renal failure reduced the intestinal absorption of calcium in primary hyperparathyroidism; 4) the ''hungry bone'' syndrome developed after parathyroidectomy in severe primary hyperparathyroidism; and 5) a target organ can fail to respond to a hormone. He also suggested that a malignant tumor could be responsible for ectopic hormone production. Finally, our review integrates the observations of Albright with our current knowledge of calcium regulation and disorders.
AuthorsA J Felsenfeld, B S Levine, C R Kleeman
JournalNefrologia : publicacion oficial de la Sociedad Espanola Nefrologia (Nefrologia) Vol. 31 Issue 3 Pg. 346-57 ( 2011) ISSN: 1989-2284 [Electronic] Spain
PMID21629339 (Publication Type: Biography, Historical Article, Journal Article, Review)
Chemical References
  • Phosphorus
  • Calcium
Topics
  • Calcium (metabolism)
  • History, 20th Century
  • Humans
  • Hyperparathyroidism, Primary (metabolism)
  • Intestinal Absorption
  • Phosphorus (metabolism)
  • Renal Insufficiency (etiology)

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